Stay Heart-Healthy with ThyroidEven low-level thyroid dysfunction, common in the elderly, is a risk factor for heart diseaseBy Will Block

he worst industrial accident in history occurred on April 26, 1986, when the nuclear reactor at Chernobyl in the Soviet Union exploded and then melted down. The huge release of ionizing radiation—100 times greater than those of the atomic bombs dropped on Hiroshima and Nagasaki—quickly killed about 2500 people and has since unleashed a plague of cancer and other illnesses on an area of Belarus, the Ukraine, and Russia occupied by about 6 million people. The full extent of this public health catastrophe will not be known for a few more decades.

The most prevalent type of cancer among the victims of Chernobyl is thyroid cancer. Why? What makes the thyroid gland so vulnerable? The answer lies in its unusual nature. Unlike the other endocrine glands, the thyroid maintains a large store—about 2 months’ worth—of the hormones it produces. Its owner can thus weather periods of reduced biosynthesis of these hormones due to insufficient dietary intake of the chemical element that makes them unique: iodine. (See the sidebar “Why We Need Iodine.”)

Why We Need Iodine

Iodine (I2) is a halogen, a highly reactive element related to fluorine, chlorine, and bromine. (Unlike the drugstore antiseptic of the same name, iodine the element is pronounced eye-oh-deen.) A bluish-black, lustrous solid at room temperature, iodine dissolves in various organic solvents to produce beautiful purple solutions. In nature it exists mainly in the form of iodide ion, I–.

It’s not accidental that the thyroid gland hoards iodine. Natural selection must have favored this development, which was vital for enabling people to survive periods of dietary iodine shortage. Iodine is relatively scarce in the earth’s soil, particularly in high mountain ranges and in certain other regions, such as the Great Lakes region and the Pacific Northwest. It’s plentiful, however, in seafood (especially shellfish) and seaweeds, such as kelp. Less important sources of iodine include milk, eggs, meat, and poultry.

In the industrialized world, most animal feeds are iodine-enriched, as is most table salt. Before iodized salt was introduced in the 1920s, the consequences of iodine deficiency—notably goiter (enlarged thyroid gland) and, in infants, the stunted physical growth and profound mental retardation of cretinism—were common.* Now they’re virtually unknown in the industrialized world, thanks to this first example of a “designer food.”

*Paradoxically, hypothyroidism and goiter can also be caused by a chronic excess of iodine, for reasons that are complicated.

With a few minor exceptions, the only part of the body that utilizes iodine for biological purposes is the thyroid, a small, bowtie-shaped gland in the front of the neck, just below the larynx. It extracts iodine efficiently from the bloodstream, incorporates it into the amino acid thyronine, and stores it in relatively large amounts for a long time. This quirk of human physiology proved disastrous for the victims of Chernobyl, who were exposed to very high levels of radioactive iodine: the “hot” atoms entered their thyroids and stayed there rather than being rapidly metabolized and excreted, as happens with most other nutrients. Children are the most vulnerable—their rate of thyroid cancer soared 10- to 30-fold within a decade of the accident.

Feeling Sluggish? Check Your Thyroid.

For the rest of us, it’s fortunate that the thyroid gland hoards its hormones, whose sustained action in our bodies is vital for our health. Their main functions are to increase metabolic rate and to increase the rate and strength of the heartbeat. Ordinarily, the levels of these hormones are tightly regulated, ensuring an even metabolic keel as we navigate life’s turbulent waters. The levels can, however, go awry: overproduction leads to hyperthyroidism, and underproduction leads to hypothyroidism. The latter is more common; women are more susceptible than men, and in both sexes the incidence increases with age.

In hypothyroidism, the hormone levels are below the normal range. Most cases of this disease are autoimmune in nature, i.e., they arise when the body turns on itself for no apparent reason and begins degrading some aspect of its own functionality—in this case, thyroid function. The principal symptom of overt hypothyroidism is a general sluggishness, both physical and mental, caused by low metabolism. More specifically, there are symptoms such as tiredness, weakness, poor memory, difficulty in concentrating, cold intolerance, constipation, dry skin, coarse hair, hair loss, and a tendency to gain weight despite poor appetite. If not treated, hypothyroidism can become dangerous, in large part because of its damaging effects on the heart.

Hypothyroidism Is Easy to Treat

Fortunately, the standard treatment is simple, safe, and highly effective: administer thyroid hormones (usually for life) to remedy the deficit. For the past half-century, the standard practice among most physicians has been to use synthetic thyroxine (T4), which is identical to natural thyroxine; the liver converts much of it to triiodothyronine (T3), the more biologically active of the two thyroid hormones. (For further information, see the sidebar “A Tale of Two Hormones.”)

A Tale of Two Hormones

There are two thyroid hormones: tetraiodothyronine, commonly called thyroxine (T4), which contains four iodine atoms, and triiodothyronine (T3), which contains three iodine atoms. Two other compounds produced by the thyroid, diiodothyronine (T2) and monoiodothyronine (T1) are chemical precursors in the synthesis of T4 and T3. They are not secreted except in negligible amounts and are not believed to have any hormonal activity, although it’s possible that some hitherto undiscovered activity may exist.

The thyroid gland’s hormone output consists predominantly of T4, and some of that is slowly converted (mainly in the liver) to T3. Thus, the large, stable “pool” of T4 acts as a kind of reservoir for the steady production of T3. Both hormones are biologically active, but T3 is about 3–4 times more active than T4.

Thyroid hormones serve three important functions: (1) regulation of cellular energy metabolism; (2) control of cell differentiation and growth; and (3) modification of the actions of other hormones, especially adrenaline and noradrenaline, which play profoundly important roles in cardiovascular function. This third function of the thyroid hormones magnifies their already pervasive influence throughout the body.

Thyroid hormones are active from fetal life to the end of life, but their greatest activity occurs in cold weather, during childhood and adolescence, during pregnancy,* and during periods of emotional stress, which can wreak biochemical havoc on many bodily systems.

*The thyroid swells during pregnancy, a fact that some African tribes exploit as an early pregnancy test. The bride is fitted with a tight but delicate necklace. As the thyroid swells, the necklace will soon break, indicating pregnancy.

What determines thyroid activity at any given time is the body’s master gland, the pituitary, which secretes (among other things) thyroid-stimulating hormone (TSH). True to its name, TSH causes the thyroid gland to produce and release thyroid hormones into the circulation. This system has an ingenious self-regulating mechanism: the thyroid hormones act on the pituitary gland, inhibiting the production of TSH. Thus, if thyroid hormone levels become too high, TSH production drops, putting the brakes on further hormone production; conversely, if the hormone levels become too low, TSH production rises, causing a boost in thyroid output.

Because this feedback loop is such a sensitive regulator of thyroid hormone levels, TSH provides a simple and useful initial diagnostic test for thyroid function. If TSH levels are normal, the thyroid hormone levels will almost certainly be normal too, and no further testing is necessary. If TSH levels are above normal and thyroid hormone levels are below normal, it indicates overt hypothyroidism (and vice versa for overt hyperthyroidism). But If TSH levels are above normal and thyroid hormone levels are within normal limits, it indicates subclinical hypothyroidism (and vice versa for subclinical hyperthyroidism).

Other physicians prefer to use the traditional natural remedy, a dried and powdered form of whole thyroid gland from domestic cattle (whose thyroid hormones are chemically identical to our own). Some patients report that whole thyroid makes them feel better than T4 alone; a long-term benefit from this therapeutic approach has not been established, however.1

Subclinical Hypothyroidism Should Be Treated Too

Much less obvious than overt hypothyroidism, but also easy to treat, is a disorder called subclinical hypothyroidism (aka mild hypothyroidism), which is believed to affect about 4% of the general population and about 10–15% of older persons, especially women.2,3 In this condition, the patient may have few or no symptoms of disease. Thyroid hormone levels are within the normal range, but there are elevated levels of thyroid-stimulating hormone (TSH), the pituitary hormone that signals the thyroid gland when to release more thyroid hormones into the circulation. If TSH is above normal while thyroid hormones are normal, it indicates a greater than normal need for more thyroid hormones—and that means that something is wrong with the thyroid.

But here’s the problem: that “something” can arise so gradually and insidiously, and it can be so ill-defined, subtle, and seemingly insignificant to most doctors—not to mention so easily misinterpreted as being due to something else (“normal aging” is a favorite catchall)—that the medical profession has, by and large, ignored it. This could be a serious mistake, however, and more and more doctors are coming to the realization that subclinical hypothyroidism (SCH) should be taken seriously and treated.4 Some of the evidence for this growing change of heart was discussed in the January 2004 issue
(“The Benefits of Whole Natural Thyroid”). Now there is more evidence—and “change of heart” may be just the phrase to describe it.

How Does SCH Affect the Heart?

Changes in heart function—bad changes—are caused by thyroid dysfunction of both major kinds: hyperthyroidism and hypothyroidism. This has been well known for at least half a century. Among the serious cardiovascular complications associated with clinical hypothyroidism are a low heart rate and a weakened heart muscle, leading to impaired circulation. Blood levels of LDL-cholesterol (the “bad cholesterol”) increase sharply, which promotes atherosclerosis, and hypertension may develop as a result of increased peripheral resistance to blood flow.

By contrast, the association between subclinical hypothyroidism and cardiovascular disease is not nearly as certain, although it’s certainly plausible.5,6 A number of epidemiological studies have investigated this question, but with conflicting results, owing perhaps to various methodological limitations, such as small size and short duration.7 New insight, however, may be gained from two studies of large size and long duration that have just been published, back-to-back, in the Archives of Internal Medicine; both give strong evidence that SCH is a risk factor for heart disease.

SCH Is a Risk Factor for Heart Disease

The first study, a Swiss-American collaboration, followed 2730 men and women, aged 70–79, for 4 years.8 The researchers were looking for a statistically significant (and presumably causal) link between SCH and any of six diseases or events: congestive heart failure, coronary heart disease, stroke, peripheral arterial disease, cardiovascular mortality, and total mortality (i.e., death from any cause). What they found was a strong link with congestive heart failure (CHF), but none of the others. The risk for CHF grew with the severity of the SCH, ranging from no increase (over normal) in mild cases to 2 1/2 times greater than normal in moderate cases to over 3 times greater in severe cases.

The second study, involving 2108 men and women, aged 17–89, was conducted in Australia over a 20-year period.5 In this study, the researchers were looking for an association between SCH and coronary heart disease (CHD), and they found it: compared with normal, healthy individuals, the risk for CHD was almost doubled in individuals with mild to moderate cases of SCH, and it was approximately tripled in those with severe SCH.

Take This to Heart

Although the two studies had opposite findings with respect to coronary heart disease, both showed a link between subclinical hypothyroidism and some form of heart disease. The author of an accompanying editorial in the journal wrote,7

Taken together, these studies suggest that the incidence of some cardiovascular disorders may be increased in patients with SH [SCH]. … The data in these studies would certainly support the idea that the treatment of severe SH with levo-thyroxine in patients younger than 80 years may be beneficial …

So perhaps, if you’re not feeling like the ball of fire you once were, and you suspect that your thyroid is the culprit, you should take that suggestion to heart—but with one twist: instead of levo-thyroxine, take whole natural thyroid, just as Mother Nature intended.